Expression data from Alzheimer's disease (AD) model mouse and AD model mouse overexpressing human mitochondrial transcriptional factor A (hTFAM). Mus musculus

To delineate the mechanism underlying the amelioration of AD pathophysiology by hTFAM, we performed gene expression profiling using hippocampal RNAs from the AD model mouse and AD model mouse overexpressing human TFAM. One-way ANOVA of microarray data from hippocampus revealed that the gene expression profile is most significantly altered in the hippocampi of ADh/hTFAMh mice. Comparative analyses of the brains of ADh/WT and ADh/hTFAMh mice showed that the expression of genes involved in cancer, endocrine system disorders, and organismal injury and abnormalities were significantly altered. Among the genes whose expression was significantly altered by hTFAM expression, transthyretin, encoded by the Ttr gene, binds Aβ and inhibits its aggregation. Overall design: Hemizygous 3xTg-AD mice harboring hemizygous APPSwe and tauP301L transgenes with a hemizygous Psen1M146V mutation (ADh/WT), and hemizygous 3xTg-AD mice with the hemizygous hTFAM transgene (ADh/hTFAMh) were used in this study, (male, n=3 for each group). RNA samples prepared from hippocampi were subjected to microarray analysis using the Affymetrix Mouse Gene 1.0 ST platform (GPL6246).